2008Tianjin yiyaoRequires access

Influence of ERK on Nerve Cell Apoptosis of Cortex Following Traumatic Brain Injury in Rats

Zhimin Zhang

Open publisher page 0 citations

Abstract

Objective: To investigate the effect of extracellular-signal regulated protein kinase (ERK) signal transduction mechanism in traumatic brain injury(TBI) in rats. Methods: The rat model of TBI was made according to the method of Marmarou(1994). A total of 92 male Sprague-Dawley rats were randomly divided into control and TBI groups. The rats in group of TBI were divided into 7 subgroups according to the time phase after brain injury,which were 10 min,30 min,3 h,6 h,24 h,48 h and 72 h. The expression of ERK was detected by immunohistochemical and Western blot methods. The expression of c-fos was detected by immunohistochemical method. The apoptosis of cortex cell was detected by TUNEL. Results: The activities of p-ERK1/2,c-fos and TUNEL positive cells were increased in TBI group compared to those in the control group. Conclusion: The excessive activation of ERK is one of mechanisms of nerve cell apoptosis by inducing c-fos protein following traumatic brain injury in rats.

About this research paper

What this paper is about

Objective: To investigate the effect of extracellular-signal regulated protein kinase (ERK) signal transduction mechanism in traumatic brain injury(TBI) in rats. Methods: The rat model of TBI was made according to the method of Marmarou(1994). A total of 92 male Sprague-Dawley rats were randomly divided into control and TBI groups. The rats in group of TBI were divided into 7 subgroups according to the time phase after brain injury,which were 10 min,30 min,3 h,6 h,24 h,48 h and 72 h. The expression of ERK was detected by immunohistochemical and Western blot methods. The expression of c-fos was detected by immunohistochemical method. The apoptosis of cortex cell was detected by TUNEL. Results: The activities of p-ERK1/2,c-fos and TUNEL positive cells were increased in TBI group compared to those in the control group. Conclusion: The excessive activation of ERK is one of mechanisms of nerve cell apoptosis by inducing c-fos protein following traumatic brain injury in rats.

Why it matters

A significance statement is not available in the OpenAlex record.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

Objective: To investigate the effect of extracellular-signal regulated protein kinase (ERK) signal transduction mechanism in traumatic brain injury(TBI) in rats. Methods: The rat model of TBI was made according to the method of Marmarou(1994). A total of 92 male Sprague-Dawley rats were randomly divided into control and TBI groups. The rats in group of TBI were divided into 7 subgroups according to the time phase after brain injury,which were 10 min,30 min,3 h,6 h,24 h,48 h and 72 h. The expression of ERK was detected by immunohistochemical and Western blot methods. The expression of c-fos was detected by immunohistochemical method. The apoptosis of cortex cell was detected by TUNEL. Results: The activities of p-ERK1/2,c-fos and TUNEL positive cells were increased in TBI group compared to those in the control group. Conclusion: The excessive activation of ERK is one of mechanisms of nerve cell apoptosis by inducing c-fos protein following traumatic brain injury in rats.

Key concepts: TUNEL assay, Traumatic brain injury, Apoptosis, MAPK/ERK pathway, Immunohistochemistry, Western blot, Cortex (anatomy), Medicine

Related papers

Back to paper searchBrowse research topicsOriginal source
Influence of ERK on Nerve Cell Apoptosis of Cortex Following Traumatic Brain Injury in Rats — Research Paper | ScholarLens